玉郎伞黄酮对心肌缺血再灌注损伤心肌组织ATP酶和凋亡蛋白的影响

吕纪华; 贺敏; 黄建春; 林兴; 黄仁彬

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玉郎伞黄酮对心肌缺血再灌注损伤心肌组织ATP酶和凋亡蛋白的影响

更新时间：2024-01-04

- 玉郎伞黄酮对心肌缺血再灌注损伤心肌组织ATP酶和凋亡蛋白的影响
- Effect of Flavonoid of Yulangsan on ATPase and Apoptosis-correlated Protein of Myocardial Ischemia-Reperfusion Injury
- 中国实验方剂学杂志 2010年16卷第13期页码：162-166
- 作者机构：
- 作者简介：
- 基金信息：
  
  广西科学研究与技术开发计划项目(桂科攻0630002-2A)
- DOI：
  中图分类号：
- 纸质出版日期：2010
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吕纪华, 贺敏, 黄建春, 等. 玉郎伞黄酮对心肌缺血再灌注损伤心肌组织ATP酶和凋亡蛋白的影响[J]. 中国实验方剂学杂志, 2010,16(13):162-166.

LV Ji-hua, HE Min, HUANG Jian-chun, et al. Effect of Flavonoid of Yulangsan on ATPase and Apoptosis-correlated Protein of Myocardial Ischemia-Reperfusion Injury[J]. Chinese journal of experimental traditional medical formulae, 2010, 16(13): 162-166.
吕纪华, 贺敏, 黄建春, 等. 玉郎伞黄酮对心肌缺血再灌注损伤心肌组织ATP酶和凋亡蛋白的影响[J]. 中国实验方剂学杂志, 2010,16(13):162-166. DOI：

LV Ji-hua, HE Min, HUANG Jian-chun, et al. Effect of Flavonoid of Yulangsan on ATPase and Apoptosis-correlated Protein of Myocardial Ischemia-Reperfusion Injury[J]. Chinese journal of experimental traditional medical formulae, 2010, 16(13): 162-166. DOI：

摘要

目的 :研究玉郎伞黄酮(FYLS)对大鼠离体心肌缺血再灌注损伤(I/R)心肌组织Na+-K+-ATP酶、Ca2+-ATP酶和凋亡蛋白的影响。方法 :离体大鼠心脏采用Langendorff法灌流

停灌30 min再灌30 min造成I/R模型。测定心肌组织Na+-K+-ATP酶、Ca2+-ATP酶活性。同时观察药物对缺血再灌注后心肌组织病理形态、凋亡相关蛋白Bcl-2

Bax表达的影响。结果 :FYLS高剂量(8×10-3g ·L-1)可显著改善缺血-再灌注所致的心功能损伤

增加Na+-K+-ATP酶、Ca2+-ATP酶的活性;与模型组比较

FYLS高剂量组病理结果显示心肌组织受损程度明显减轻(P<0.05)

且明显降低心肌Bax蛋白表达(P<0.01)

对Bcl-2蛋白表达无明显影响

但能显著增加Bcl-2/Bax的比率(P<0.05)。结论 :FYLS对I/R具有保护作用

其机制可能与减轻钙超载、下调Bax蛋白表达、增加Bcl-2/Bax的比率有关。

Abstract

Objective: To study the effect and mechanism of flavonoid of Yulangsan (FYLS) on the activities of Na+-K+-ATPase and Ca2+-ATPase and the apoptosis-correlated proteins of myocardial ischemia-reperfusion injury (I/R) in isolated rat hearts. Method: Langendorff-perfusion Isolated rat hearts were prepared. I/R was induced by 30 minutes global ischemia followed by 30 minutes reperfusion. The activities of Na+-K+-ATPase and Ca2+-ATPase in myocardial tissues were determined. The pathological changes of myocardium and the expressions of apoptosis-correlated protein Bcl-2 and Bax were analyzed. Result: High dose of FYLS(8×10-3g ·L-1)could increase the activities of Na+-K+-ATPase and Ca2+-ATPase. Histopathological examination confirmed that the degree of myocardial injury in high dose of FYLS group was obviously lessened when compared with I/R group (P<0.05). FYLS could downregulate the expression of Bax (P<0.01) and significantly increase the ratio of Bcl-2/Bax (P<0.05). Conclusion: FYLS may offer myocardial protective effect against I/R

which may be related to its effects of reducing calcium overload

downregulating the expression of Bax protein

and increasing the Bcl-2/Bax ratio.

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